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TRAILBLAZER-ALZ

Donanemab in Early Alzheimer's Disease

Year of Publication: 2021

Authors: Mark A. Mintun, Albert C. Lo, Cynthia Duggan Evans, ..., Daniel M. Skovronsky

Journal: New England Journal of Medicine

Citation: N Engl J Med 2021;384:1691-1704

Link: https://doi.org/10.1056/NEJMoa2100708


Clinical Question

Does donanemab, an antibody targeting deposited N-terminal pyroglutamate amyloid-β plaques, slow cognitive and functional decline in patients with early symptomatic Alzheimer's disease who have confirmed tau and amyloid pathology on PET?

Bottom Line

Donanemab met the primary endpoint, showing 32% less decline on iADRS vs placebo at 76 weeks (P=0.04), but fell short of the prespecified goal of 50% slowing. The key secondary endpoint (CDR-SB) was not significant, causing the testing hierarchy to fail. Donanemab achieved robust amyloid clearance (67.8% amyloid-negative by 76 weeks) but did not significantly affect global tau load or hippocampal volume. ARIA-E occurred in 26.7% of donanemab patients. As a phase 2 trial with 257 patients, the results were promising but insufficient to establish clinical efficacy, leading to the larger TRAILBLAZER-ALZ 2 phase 3 trial.

Major Points

  • TRAILBLAZER-ALZ was a phase 2, randomized, double-blind, placebo-controlled trial of donanemab in 257 patients with early symptomatic AD across 56 sites in the US and Canada
  • Unique enrollment criteria required both tau PET (flortaucipir, intermediate range SUVR 1.10–1.46) and amyloid PET (florbetapir, ≥37 centiloids) positivity, selecting a narrower AD population with confirmed dual pathology but excluding high-tau (advanced) disease
  • Primary endpoint met: iADRS decline was −6.86 with donanemab vs −10.06 with placebo (difference 3.20; 95% CI 0.12–6.27; P=0.04), representing 32% slowing but not meeting the prespecified 50% goal
  • Key secondary endpoint CDR-SB was not significant (difference −0.36; 95% CI −0.83 to 0.12), causing the hierarchical testing procedure to fail; no definitive conclusions from remaining secondary outcomes
  • ADAS-Cog13 showed a nominally significant difference (−1.86; 95% CI −3.63 to −0.09), but ADCS-iADL (1.21; 95% CI −0.77 to 3.20) and MMSE (0.64; 95% CI −0.40 to 1.67) did not
  • Donanemab achieved rapid and substantial amyloid clearance: 85-centiloid reduction vs placebo at 76 weeks; 40% amyloid-negative by 24 weeks, 59.8% by 52 weeks, 67.8% by 76 weeks
  • Innovative dose-adjustment protocol: donanemab was reduced or switched to placebo based on amyloid PET clearance milestones (54.7% switched to placebo by week 56)
  • No significant effect on global tau load on flortaucipir PET, though prespecified regional analyses suggested reduced tau accumulation in frontal and temporal lobes
  • Greater decrease in whole-brain volume and greater increase in ventricular volume with donanemab vs placebo; no significant change in hippocampal volume
  • ARIA-E occurred in 26.7% of donanemab patients vs 0.8% placebo; symptomatic ARIA-E in 6.1%; higher incidence in ApoE ε4 carriers (ε4/ε4: 44.0%, ε3/ε4: 30.9%, ε3/ε3: 11.4%)
  • Antidrug antibodies detected in approximately 90% of donanemab-treated participants
  • A combination-therapy arm (donanemab + BACE1 inhibitor LY3202626) was discontinued early due to futility in a separate phase 2 trial of the BACE1 inhibitor

Design

Study Type: Randomized, double-blind, placebo-controlled, multicenter phase 2 trial

Randomization: 1

Blinding: Double-blind. Safety assessments performed by site investigators unaware of group assignments. Efficacy raters were trained and unaware of trial group assignments. Unblinded florbetapir PET results used to guide dose adjustments per protocol.

Enrollment Period: Not explicitly stated; ClinicalTrials.gov NCT03367403 (registered December 2017)

Follow-up Duration: 76 weeks (72 weeks of dosing + 4 weeks to final assessment)

Centers: 56

Countries: United States, Canada

Sample Size: 257

Analysis: Modified intention-to-treat (baseline + ≥1 postbaseline iADRS score). Primary analysis: MMRM with fixed effects for baseline score, investigator, trial group, visit, trial group × visit, baseline score × visit, concomitant acetylcholinesterase inhibitor/memantine use, and age. Hierarchical testing (Bretz-Maurer graphical approach) for type I error control across primary and key secondary endpoints (CDR-SB tested first at full alpha; remaining propagated). Bayesian disease progression model as supplementary analysis (diffuse priors, posterior probability of ≥25% slowing as prespecified positive outcome). Fisher's exact test for categorical comparisons. ANCOVA for continuous data at 76 weeks. Missing data handled by likelihood-based MMRM.


Inclusion Criteria

  • Age 60–85 years
  • Early symptomatic Alzheimer's disease: prodromal AD (MCI) or mild AD with dementia
  • MMSE score 20–28
  • Flortaucipir (18F) PET showing tau deposition consistent with AD pattern, with SUVR between 1.10 and 1.46 (intermediate tau; excluding high-tau/advanced disease and low-tau/non-AD)
  • Florbetapir (18F) PET amyloid positive (SUVR ≥1.17, equivalent to ≥37 centiloids)
  • Patients with SUVR <1.10 but topographic pattern consistent with advanced AD were included

Exclusion Criteria

  • Tau SUVR >1.46 on flortaucipir PET (high tau/advanced disease)
  • Tau SUVR <1.10 with deposition pattern not consistent with AD
  • Amyloid SUVR <1.17 on florbetapir PET (<37 centiloids)
  • Other specific exclusion criteria per protocol (not fully detailed in publication)

Arms

FieldControlDonanemab
InterventionMatching placebo IV infusion every 4 weeks for up to 72 weeksDonanemab 700 mg IV for first 3 doses then 1400 mg IV every 4 weeks for up to 72 weeks. Dose reduced to 700 mg if amyloid PET 11–<25 centiloids; switched to placebo if amyloid PET <11 centiloids on one scan or 11–<25 centiloids on two consecutive scans. Dose not escalated if ARIA-E occurred during first 3 doses.
Duration72 weeks (final assessment at 76 weeks)72 weeks (final assessment at 76 weeks)

Outcomes

OutcomeTypeControlInterventionHR / OR / RRP-value
Change from baseline to 76 weeks in iADRS score (Integrated Alzheimer's Disease Rating Scale; range 0–144, lower = greater cognitive and functional impairment; composite of ADAS-Cog13 and ADCS-iADL)Primary−10.06−6.860.04
CDR-SB change from baseline at 76 weeks (key secondary; range 0–18, higher = greater impairment)SecondaryNot separately reportedNot separately reportedNot significant (hierarchy failed)
ADAS-Cog13 change from baseline at 76 weeks (range 0–85, higher = greater deficit)SecondaryNot separately reportedNot separately reportedNominal (hierarchy failed at CDR-SB)
ADCS-iADL change from baseline at 76 weeks (range 0–59, lower = greater impairment)SecondaryNot separately reportedNot separately reportedNot significant
MMSE change from baseline at 76 weeks (range 0–30, higher = better)SecondaryNot separately reportedNot separately reportedNot significant
Amyloid plaque level on florbetapir PET at 76 weeks (centiloids)Secondary+0.93 centiloids−84.13 centiloidsSignificant (not explicitly stated)
Amyloid-negative status (<24.10 centiloids) at 76 weeks in donanemab groupSecondary
Global tau load on flortaucipir PET change from baseline to 76 weeksSecondaryNot significant
Bayesian disease progression ratio (iADRS)Secondary
ARIA-EAdverse0.8% (1/125)26.7% (35/131)<0.001
ARIA-E symptomaticAdverse0.8%6.1%
ARIA-E by ApoE genotype (donanemab)Adverse
ARIA-H (any)Adverse7.2% (9/125)30.5% (40/131)
ARIA-H microhemorrhageAdverse4.8% (6/125)19.8% (26/131)
Superficial siderosisAdverse3.2% (4/125)13.7% (18/131)0.003
MacrohemorrhageAdverse0%0%
HeadacheAdverse12.0%7.6%0.29
FallAdverse15.2%13.0%0.72
NauseaAdverse3.2%10.7%0.03
Infusion-related reactionAdverse0%7.6%0.002
Serious adverse eventsAdverse17.6%17.6%>0.99
DeathAdverse1.6% (2/125)0.8% (1/131)0.62
Discontinuation of intervention due to AEAdverse7.2%30.5%<0.001
Discontinuation of trial due to AEAdverse4.8%15.3%0.007

Subgroup Analysis

Not formally reported in this publication. Bayesian disease progression model analyses showed similar estimates of treatment effect across iADRS, CDR-SB, ADAS-Cog13, ADCS-iADL, and MMSE, though credible intervals were wide and not adjusted for multiple comparisons. Participants with and without ARIA-E appeared to have similar iADRS trajectories by visual inspection of curves.


Criticisms

  • Small sample size (n=257) limits statistical power and generalizability; the trial was powered for a 50% slowing that was not achieved (only 32% observed)
  • Key secondary endpoint CDR-SB was not significant, causing hierarchical testing failure; thus no confirmed clinical benefit beyond the composite iADRS primary endpoint
  • The iADRS is a relatively newer composite endpoint not universally accepted as a standard in AD trials; the 3.20-point difference on a 144-point scale has uncertain clinical meaningfulness
  • Very limited racial/ethnic diversity (93–96% White, <4% Black), severely limiting generalizability
  • High rate of treatment discontinuation due to AEs in donanemab group (30.5% vs 7.2%), introducing potential survivor bias
  • ARIA-E occurrence may have led to functional unblinding despite blinded rater design
  • No significant effect on global tau load despite robust amyloid clearance, questioning whether amyloid removal translates to modification of downstream disease pathology within the study timeframe
  • Paradoxical findings on volumetric MRI: greater whole-brain volume loss and ventricular enlargement with donanemab despite clinical benefit signal; mechanism unclear
  • Dose heterogeneity due to ARIA-E–related dose holds and amyloid PET–based dose reduction/placebo switch complicates interpretation
  • Antidrug antibody development in ~90% of participants raises questions about long-term efficacy and retreatment feasibility
  • All authors with potential conflicts of interest: most are Eli Lilly employees and shareholders; trial designed, funded, and analyzed by Eli Lilly
  • COVID-19 pandemic led to some telephone visits replacing on-site visits, with no efficacy data collected at those visits

Funding

Eli Lilly. Eli Lilly designed and funded the trial, provided donanemab and placebo, analyzed the data, and provided professional writing assistance in drafting the manuscript.

Based on: TRAILBLAZER-ALZ (New England Journal of Medicine, 2021)

Authors: Mark A. Mintun, Albert C. Lo, Cynthia Duggan Evans, ..., Daniel M. Skovronsky

Citation: N Engl J Med 2021;384:1691-1704

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